Noninvasive central venous pressure measurement by controlled compression sonography at the forearm.

OBJECTIVES: We sought to validate a new noninvasive technique to determine central venous pressure (CVP) using high-resolution compression sonography. BACKGROUND: Information concerning CVP is crucial in clinical situations, including cardiac failure, volume overload, and sepsis. The measurement of CVP, however, requires puncture of a vein with attendant risk of complication. METHODS: After a proof-of-concept study in healthy subjects, a prospective blinded evaluation was performed comparing CVP measurement using a central venous catheter with measurement using compression sonography in critically ill (intensive care unit) patients. RESULTS: In healthy subjects with experimentally induced venous hypertension with a wide range of pressure values, a strong correlation (r = 0.95; p < 0.001) between noninvasive and invasive peripheral venous pressure at the forearm was shown. High interobserver agreement with an intraclass correlation coefficient of 0.988 shows excellent reliability of the system. Noninvasive peripheral venous pressure measurement at the forearm showed a good correlation with CVP in 50 intensive care unit patients with the forearm positioned both below heart level (r = 0.84; p < 0.001) and at heart level (r = 0.85; p < 0.001). The mean difference between invasive and noninvasive measurement was negligible (-0.1 +/- 3.5 cm H2O and -0.7 +/- 3.4 cm H2O, respectively). CONCLUSIONS: Controlled-compression sonography is a valuable tool for measuring venous pressure in peripheral veins and allows reliable indirect assessment of CVP without intravenous catheterization.     

Enhanced sensitivity to oxidant-induced micronucleus frequency in elderly individuals is not associated with glutathione S-transferase M1 (GSTM1) null genotype in lymphocytes

BACKGROUND: A large number of studies have demonstrated that various kinds of DNA damage accumulate during aging and that oxidative stress possibly contributes to this process. Glutathione S-transferase M1 (GSTM1) can prevent their possible effects on DNA via detoxification of reactive substances that induced oxidative stress. OBJECTIVE: To investigate the relationship between GSTM1 polymorphism and DNA sensitivity to oxidative stress with age, we used micronucleus (MN) frequency as a marker of DNA damage in lymphocytes from young and elderly subjects. Methods: This study was performed in 30 young (age range 20-36 years) and 30 elderly (age range 66-87 years) healthy individuals who were chosen on the basis of their GSTM1 genotype (15 GSTM1 null and 15 GSTM1 positive for each group). Lymphocytes were cultured after Ficoll isolation and treated for 48 h with a 30-muM dose of cumene hydroperoxide (CumOOH), a dose that does not decrease cell viability. RESULTS: There was no significant difference in the MN frequency observed in control cultures from young and elderly individuals. However, the MN frequency in CumOOH-treated cultures was significantly higher in the elderly group than the young group (p < 0.001). No association was found between the GSTM1 phenotype and CumOOH-induced MN frequency. CONCLUSIONS: The results suggest that lymphocytes of elderly individuals are more susceptible to in vitro MN induction by CumOOH. However, this difference in susceptibility is not explained by the lack of GSTM1.     

Reactive oxygen species and chemokines： Are they elevated in the esophageal mucosa of children with gastroesophageal reflux disease？

AIM： To determine the role of inflammatory cytokines and reactive oxygen species （ROS） in childhood reflux esophagitis. METHODS： A total of 59 subjects who had complaints suggesting GERD underwent esophagogastroduoden oscopy. Endoscopic and histopathologic diagnosis of reflux esophagitis was established by Savary-Miller and Vandenplas grading systems, respectively. Esophageal biopsy specimens were taken from the esophagus 20% proximal above the esophagogastric junction for conventional histopathological examination and the measurements of ROS and cytokine levels. ROS were measured by chemiluminescence, whereas IL-8 and MCP-1 levels were determined with quantitative immunometric ELISA on esophageal tissue. Esophageal tissue ROS, IL-8 and MCP-1 levels were compared among groups with and without endoscopic/histo- pathologic esophagitis. RESULTS： Of 59 patients 28 （47.5%） had normal esophagus whereas 31 （52.5%） had endoscopic esophagitis. In histopathological evaluation, almost 73% of the cases had mild and 6.8% had moderate degree of esophagitis. When ROS and chemokine levels were compared among groups with and without endoscopic esophagitis, statistical difference could not be found between patients with and without esophagitis. Although the levels of ROS, IL-8 and MCP-1 were found to be higher in the group with histopathological reflux esophagitis, this difference was not statistically significant. CONCLUSION： These results suggest that the grade of esophagitis is usually mild or moderate during childhood and factors apart from ROS, IL-8 and MCP-1 may be involved in the pathogenesis of reflux esophagitis in children.     

A Chryseobacterium meningosepticum outbreak observed in 3 clusters involving both neonatal and non-neonatal pediatric patients

Three clusters of Chryseobacterium meningosepticum infections in a tertiary health center in July 2006 and January 2007 involving 8 newborns and 5 older children were investigated. The index patient was from the neonatal intensive care unit, and the older patients were from other pediatric wards. Cultures were obtained from the environment and from health care workers' hands as part of an outbreak investigation. C meningosepticum was isolated from hand cultures obtained from a senior resident and from environmental cultures obtained from powdered infant formula, an electrical button, a computer keyboard, phone, a doorknob, and an Ambu bag. Antibiogram typing and enterobacterial repetitive intergenic consensus sequence polymerase chain reaction indicated that all of the isolates were epidemiologically related. Nine patients improved on antimicrobial treatment, and 4 premature infants died after the infection. C meningosepticum is a well-known etiologic agent for nosocomial infections involving newborns and immunocompromised patients. Wet and dry environmental surfaces and equipment may act as a source or play a role in disseminating the microorganism. Outbreaks may be controlled with strong emphasis on infection control measures.     

In vivo effect of losartan on platelet aggregation in patients with hypertension

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 ± 12.8 and 149.2 ± 17.3mmHg, respectively. Mean DBP decreased from 93.7 ± 8.2 to 87.7 ± 10.3mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% ± 24.3% before and 58.3% ± 18.1% after the treatment. The same variables with ristocetin were 66.8% ± 21.6% and 60.8% ± 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.     

Serum lipid and leptin concentrations in hypopituitary patients with growth hormone deficiency

OBJECTIVE: To investigate the effects of growth hormone (GH) deficiency on serum lipid and leptin concentrations in hypopituitary patients taking conventional replacement therapy and to determine the relations between leptin and gender and anthropometric and metabolic variables. SUBJECTS: Twenty-one GH deficient adult hypopituitary patients (15 women, six men) and 21 (14 women, seven men) age, sex and body mass index (BMI) matched healthy controls. MEASUREMENTS: After an overnight fast, anthropometric parameters were measured and body composition was determined by a bioelectrical impedance analyser. Venous blood samples were obtained for the measurements of glucose, total cholesterol, high density lipoprotein (HDL) cholesterol, triglyceride, intact insulin, insulin-like growth factor 1 (IGF-1) and leptin concentrations. Serum leptin and hormones were analysed by radioimmunoassay. RESULTS: Hypopituitary patients with GH deficiency showed significantly higher triglyceride, total and low density lipoprotein (LDL) cholesterol and lower HDL cholesterol concentrations on conventional replacement therapy. The unfavourable lipid profile was particularly evident in women. Significantly higher leptin concentrations were found in patients compared with healthy controls with similar body fat content (23. 5+/-11.8 ng/ml vs 11.7+/-6.9 ng/ml, P=0.01). This difference remained significant even when leptin values were expressed in relation to fat mass percentage (0.79+/-0.40 vs. 0.42+/-0.17 ng/ml%, P<0.05) and fat mass kg (1.32+/-0.81 vs 0.66+/-0.30 ng/ml kg, P<0. 05). Significant positive correlations were observed between leptin concentrations and body fat percentage and age in the control group. In patients the sole significant relation between leptin and study parameters was the positive correlation observed between leptin and total cholesterol concentrations. Serum leptin concentrations were significantly higher in women than men in the control group, but not in the patients. No significant gender difference was observed when leptin concentrations were expressed in relation to fat mass (percentage and kg). CONCLUSION: Growth hormone deficient hypopituitary patients (particularly women) on conventional replacement therapy have a more atherogenic lipid profile. Leptin concentrations are increased in GH deficient adults even after adjustment for percentage body fat and body fat mass (kg). Although the nature of our data does not allow us to draw any conclusions on the mechanism(s) of increased leptin concentrations in GH deficiency, decreased central sensitivity to leptin and increased leptin production from per unit fat mass, or alterations in leptin clearance, might be operative.     

Pinealectomy exaggerates and melatonin treatment suppresses neuroma formation of transected sciatic nerve in rats: gross morphological, histological and stereological analysis

At present, an intensive effort for prevention of neuroma formation following peripheral nerve section continues. It has been recently suggested that surgical pinealectomy (Px) induces elevation of the collagen content in the granulation tissue of a wound, while melatonin application after Px suppresses elevation of the collagen accumulation in the tissue. The aim of the present study was to assess whether melatonin had the ability to suppress collagen production and neuroma formation following peripheral nerve transection. A total of 40 male rats (four groups of 10) were left intact (intact controls) or sham operated (sham group), were Px, or were Px and given melatonin (Px + melatonin group). All animals underwent a surgical intervention consisting of right sciatic nerve neurectomy. After 4 wk, the animals were killed following intracardiac perfusion. Gross morphology of neuroma formation in the proximal nerve segment was examined and proximal neuroma evaluated. Macroscopic and microscopic findings revealed that Px caused a proliferation of connective tissue and large neuroma formation at the proximal ends of transected nerves. Stereological analysis showed that there was a statistically significant reduction in connective tissue content of the same region in Px animals treated with melatonin (P < 0.005). The results achieved in a rodent model of sciatic nerve neuroma formation showed that there was a positive correlation between macroscopic and microscopic observations, and that melatonin enhanced axonal regeneration presumably due to its inhibitory effect on neuroma formation.     

Brachial plexus injury during open heart surgery--controlled prospective study

BACKGROUND: Postoperative brachial plexus injury is often reported because the brachial plexus is stretched by sternotomy and the use of sternal retractors during open heart surgery. In many studies, brachial plexus injuries have been demonstrated by postoperative electrophysiological studies in susceptible patients. In this study, we estimated the incidence, severity, and type of brachial plexus injuries by routine preoperative and postoperative electrophysiological studies of patients undergoing open heart surgery. METHODS: Patients undergoing coronary artery bypass grafting (CABG) surgery (Group 1), heart valve surgery (Group 2), or peripheral vascular surgery (Group 3) were included in the investigation. Electrophysiological studies of both upper extremities were performed five days before and three weeks after the operation. RESULTS: Peripheral nerve problems were found preoperatively in 23 of the 112 patients (21 %). These problems persisted, but similar findings were obtained postoperatively from the left upper extremities of six of the 42 CABG (14 %) and two of the 24 heart valve (8 %) patients who had had normal preoperative evaluations. The patients with injured nerves were older and had undergone longer operation times. There were no differences between the patients with injured nerves and the others with respect to mammary artery harvesting or other operative variables. CONCLUSIONS: There are no reports in the literature of routine preoperative and postoperative electrophysiological studies in large patient groups to evaluate brachial plexus injury during open heart surgery. It is known that heart surgery sometimes causes partial brachial plexus injury, especially in the lower trunk. However, these peripheral nerve problems are usually not considered clinically important and are not investigated. Patients undergoing open heart surgery must be closely followed up for peripheral nerve injury during the postoperative period.     

Preliminary study showing the relationship between platelet fibronectin, sialic acid, and ADP-induced aggregation levels in coronary heart disease.

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.